Made available in DSpace on 2016-12-06T17:06:55Z (GMT). No. of bitstreams: 1 Rafael Alves de Aguiar.pdf: 1586651 bytes, checksum: 8d04dd9879dde565cc4689f0800acf3b (MD5) Previous issue date: 2013-06-04 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior / The aim of this study was to determine the mode and the level that the physiological and performance variables influence in repeated running sprint ability. To this end, the study used 27 males participants (10 sprint runners (VEL), 8 long-distance runners (FUN) and 9 active subjects (ATI)). In a synthetic track these subjects were submitted to following tests on different days: 1) Incremental testing for determination of VO2max and maximal aerobic velocity (MAV); 2) constant velocity test at 110%MAV for determination of on- and off transition kinetics of VO2 and accumulated deficit oxygen (AOD); 3; 1 minute all-out test for determination of blood lactate concentration ([lac]s) kinetics and off-transition kinetics of VO2; and 4) repeated sprint test (10 sprints of 35 m departing every 20 s) for determine the total time of sprints, best sprint and percentage decrement score (Sdec). In every tests the [lac]s and blood pH were analyzed for observe the difference between maximal value after exercise and rest value (i.e. ∆[lac]s e ∆pH).Total time was significant different between all groups (VEL, 49,5 ± 0,9 s; FUN, 52,6 ± 3,1 s; ATI, 55,9s ± 2,6 s) and Sdec was significant lower in long distance runners compared to other groups (VEL, 8,5 ± 2,5%; FUN, 4,0 ± 2,0%; ATI, 8,3 ± 4,1%). Total time was significant correlated with best sprint (r 0,86), AOD in T110 (r = -,061) and T1min (r = -0,60), ∆[lac]s (r = -0,64) and ∆pH (r = 0,59) in RS, primary time constant (tau1) (r = -0,45) e O2 consumed in fast component after exercise in T1min (r = -0,44). Differently, Sdec was significant correlated with aerobic variables (VO2max, r = -0,59; MAV, r = -0,55; tau1 during exercise, r = 0,41), tau1 after T110 (r = 0,59) and T1min (r = 0,47), as well as, with lactate exchange ability (r 0,75). Therefore, it was concluded that repeated sprint performance is strongly influenced by anaerobic characteristics, while mechanisms related to removal of metabolites originated by anaerobic metabolism and aerobic indices influence to decrease fatigue in RS. / O objetivo deste estudo foi determinar o modo e o grau que as variáveis fisiológicas e de desempenho influenciam no desempenho em sprints repetidos. Para este fim, participaram do estudo 27 homens, sendo 10 corredores velocistas (VEL), 8 corredores fundistas (FUN) e 9 sujeitos ativos (ATI). Em uma pista sintética de atletismo estes sujeitos foram submetidos, em dias diferentes, aos seguintes testes: 1) teste incremental para determinação do VO2max e da velocidade aeróbia máxima (MAV); 2) teste de velocidade constante realizado a 110%MAV (T110) para determinar a cinética do VO2 durante e após o exercício e o déficit de oxigênio (AOD); 3) teste de um minuto máximo (T1min), para determinar a cinética da concentração de lactato sanguíneo ([lac]s) e a cinética do VO2 após o exercício; e 4) teste de sprints repetidos (RS) (10 sprints de 35m, intercalados com 20s de recuperação) para determinar o tempo total dos sprints, melhor sprint e a queda do escore em percentual (Sdec). Em todos os testes a [lac]s e o pH sanguíneo foram analisados para observar a diferença entre o valor máximo após o exercício e o valor de repouso (i.e. ∆[lac]s e ∆pH). Tempo total em RS foi significativamente diferente entre todos os grupos (VEL, 49,5 ± 0,9 s; FUN, 52,6 ± 3,1 s; ATI, 55,9s ± 2,6 s) e Sdec foi significativamente inferior em fundistas comparado aos outros grupos (VEL, 8,5 ± 2,5%; FUN, 4,0 ± 2,0%; ATI, 8,3 ± 4,1%). Tempo total foi correlacionado significativamente com o melhor sprint (r = 0,86), com o AOD no T110 (r = -0,61) e no T1min (r = -0,60), com o ∆[lac]s (r = -0,64) e ∆pH (r = 0,59) do RS, com a constante de tempo primária (tau1) (r = -0,45) e O2 consumido pelo componente rápido após o exercício no T1min (r = -0,44). Diferentemente, o Sdec foi correlacionado significativamente com variáveis aeróbias (VO2max, r = -0,59; MAV, r = -0,55; tau1 durante T110, r = 0,41), tau1 após T110 (r = 0,59) e T1min (r = 0,47), bem como, com a constante de tempo da entrada do lactato no compartimento sanguíneo no T1min (r = -0,75). Portanto, foi concluído que o desempenho em sprints repetidos é altamente influenciado por características anaeróbias, enquanto, mecanismos relacionados à remoção dos metabólitos originados pelo metabolismo anaeróbio e índices aeróbios influenciam para diminuir a fadiga em RS.

The current understanding of lactate metabolism in fish is based almost entirely on interpretation of concentration measurements that cannot be used to infer changes in flux. Moreover, the transporters regulating these fluxes have never been characterized in rainbow trout. My goals were: (1) to quantify lactate fluxes in rainbow trout under normoxic resting conditions, during acute hypoxia, and exercise by continuous infusion of [U-14C] lactate; (2) to determine lactate uptake capacity of trout tissues by infusing exogenous lactate in fish rest and during graded exercise, and (3) to clone monocarboxylate transporters (MCTs) and determine the effects of exhausting exercise on their expression. Such information could prove important to understand the mechanisms underlying the classic “lactate retention” seen in trout white muscle after intense exercise. In normoxic resting fish, the rates of appearance (Ra) and disappearance (Rd) of lactate were always matched (~18 to 13 µmol kg-1 min-1), thereby maintaining a low baseline blood lactate concentration (~0.8 mM). In hypoxic fish, Ra lactate increased from baseline to 36.5 µmol kg-1 min-1, and was accompanied by an unexpected 52% increase in Rd reaching 30.3 µmol kg-1 min-1, accounting for a rise in blood lactate to 8.9 mM. In exercising fish, lactate flux was stimulated > 2.4 body lengths per second (BL s-1). As the fish reached critical swimming speed (Ucrit), Ra lactate was more stimulated (+67% to 40.4 μmol kg-1 min-1) than Rd (+41% to 34.7 μmol kg-1 min-1), causing an increase in blood lactate to 5.1mM. Fish infused with exogenous lactate stimulated Rd lactate by 300% (14 to 56 μmol kg-1 min-1) during graded exercise, whereas the Rd in resting fish increased by only 90% (21 to 40 µmol kg-1 min-1). Four MCT isoforms were partially cloned and characterized in rainbow trout: MCT1b was the most abundant in heart, and red muscle, but poorly expressed in gill and brain where MCT1a and MCT2 were prevalent. MCT4 was more expressed in the heart. Transcript levels of MCT2 (+260%; brain), MCT1a (+90%; heart) and MCT1b (+50%; heart) were stimulated by exhausting exercise. This study shows that: (i) the increase in Rd lactate plays a strategic role in reducing the lactate load imposed on the circulation. Without this response, blood lactate accumulation would double; (ii) a high capacity for lactate disposal in rainbow trout tissues is elicited by the increased blood-to-tissue lactate gradient when extra lactate is administered; and (iii) rainbow trout may be unable to release large lactate loads rapidly from white muscle after exhausting exercise (lactate retention) because they poorly express MCT4 in white muscle and fail to upregulate its expression during exercise.

The current understanding of lactate metabolism in fish is based almost entirely on interpretation of concentration measurements that cannot be used to infer changes in flux. Moreover, the transporters regulating these fluxes have never been characterized in rainbow trout. My goals were: (1) to quantify lactate fluxes in rainbow trout under normoxic resting conditions, during acute hypoxia, and exercise by continuous infusion of [U-14C] lactate; (2) to determine lactate uptake capacity of trout tissues by infusing exogenous lactate in fish rest and during graded exercise, and (3) to clone monocarboxylate transporters (MCTs) and determine the effects of exhausting exercise on their expression. Such information could prove important to understand the mechanisms underlying the classic “lactate retention” seen in trout white muscle after intense exercise. In normoxic resting fish, the rates of appearance (Ra) and disappearance (Rd) of lactate were always matched (~18 to 13 µmol kg-1 min-1), thereby maintaining a low baseline blood lactate concentration (~0.8 mM). In hypoxic fish, Ra lactate increased from baseline to 36.5 µmol kg-1 min-1, and was accompanied by an unexpected 52% increase in Rd reaching 30.3 µmol kg-1 min-1, accounting for a rise in blood lactate to 8.9 mM. In exercising fish, lactate flux was stimulated > 2.4 body lengths per second (BL s-1). As the fish reached critical swimming speed (Ucrit), Ra lactate was more stimulated (+67% to 40.4 μmol kg-1 min-1) than Rd (+41% to 34.7 μmol kg-1 min-1), causing an increase in blood lactate to 5.1mM. Fish infused with exogenous lactate stimulated Rd lactate by 300% (14 to 56 μmol kg-1 min-1) during graded exercise, whereas the Rd in resting fish increased by only 90% (21 to 40 µmol kg-1 min-1). Four MCT isoforms were partially cloned and characterized in rainbow trout: MCT1b was the most abundant in heart, and red muscle, but poorly expressed in gill and brain where MCT1a and MCT2 were prevalent. MCT4 was more expressed in the heart. Transcript levels of MCT2 (+260%; brain), MCT1a (+90%; heart) and MCT1b (+50%; heart) were stimulated by exhausting exercise. This study shows that: (i) the increase in Rd lactate plays a strategic role in reducing the lactate load imposed on the circulation. Without this response, blood lactate accumulation would double; (ii) a high capacity for lactate disposal in rainbow trout tissues is elicited by the increased blood-to-tissue lactate gradient when extra lactate is administered; and (iii) rainbow trout may be unable to release large lactate loads rapidly from white muscle after exhausting exercise (lactate retention) because they poorly express MCT4 in white muscle and fail to upregulate its expression during exercise.